Although it has an enormous impact on public health, we have only limited knowledge of the molecular mechanisms underlying influenza A virus (IAV) ability to evade the immune response. Antigenic drift precludes long lasting natural or vaccine induced immunity, and is the cause of yearly vaccine reformulation. Despite its importance, we also are limited in our understanding of the molecular mechanisms underlying antigenic drift of IAV and the fine specificity of the B cell response to the IAV hemagglutinin. We are examining the changes in the structure and function of the influenza HA that provide an advantage in the face of the host neutralizing antibody response. This year we have continued to examine the breadth of the B cell repertoire in response to an influenza virus infection as well as characterizing escape from HA stem-directed monoclonal antibody pressure.